Impact of extracorporeal shock waves on the human skin with cellulite: a case study of an unique instance

Abstract

In this case study of an unique instance, effects of medium-energy, high-focused extracorporeal generated shock waves (ESW) onto the skin and the underlying fat tissue of a cellulite afflicted, 50-year-old woman were investigated. The treatment consisted of four ESW applications within 21 days. Diagnostic high-resolution ultrasound (Collagenoson) was performed before and after treatment. Directly after the last ESW application, skin samples were taken for histopathological analysis from the treated and from the contra-lateral untreated area of skin with cellulite. No damage to the treated skin tissue, in particular no mechanical destruction to the subcutaneous fat, could be demonstrated by histopathological analysis. However an astounding induction of neocollageno- and neoelastinogenesis within the scaffolding fabric of the dermis and subcutis was observed. The dermis increased in thickness as well as the scaffolding within the subcutaneous fat-tissue. Optimization of critical application parameters may turn ESW into a noninvasive cellulite therapy.

Figures

Figure 1

Shock-wave: its physics and main biological effects. a) A shock wave is a single, positive pressure pulse rising from surrounding’s pressure followed by an exponential descent and a tensile amplitude below surrounding’s pressure. The rising occurs within nanoseconds to large amplitude up to 10–100 MPa, whereas the tensile amplitude is of long duration of 2000 nsec with a comparatively small negative pressure peak between 10% to 20% of positive pressure peak. b) and c) In overcoming the cohesive forces of fluid cavitation bubbles are generated or enlarged by the shock-wave’s tensile wave component (even in the case of a negative pressure peak of less than 1 MPa). The bubbles may grow to achieve radii of more than 30 μm. These cavitation bubbles collapse after the shock-wave propagated further and surrounding’s pressure is re-established. Subsequent jet-streams can arise with velocities as large as 800 m/sec. d) The energy loss at acoustic impedance interfaces between tissues (Table 1) and even at sub-cellular structures (Bereiter-Hahn and Blase 2003; Lemor et al 2004) by refraction and diffraction contribute to the biological effect of ESW (Table 2).

Figure 2

Inner structure of the female skin and the underlying subcutaneous tissue. Partitioned border zone between corium and subcutis. The plane of the subcutis with papillae adiposae rising into dells (valley-like) and pits (hole-like) on the undersurface of the corium. Modified from Nürnberger and Müller 1978.

Figure 3

LCCT (Liquid crystal contact thermography, RW27ST with colors corresponding to temperature steps of 0.70 Celsius) of left, proximal, lateral thigh: before 1st ESW-application (control, left), immediately after 3rd ESW-application (middle) and before 4th ESW-application (right). Note the hyperemia at the site of ESW-treatment.

Figure 4

High-frequency high-resolution ultrasound measurement of skin (Collagenoson®) of left thigh before treatment (control) and after treatment (same site). Treatment: medium-energy, high focused ESW. Notice: increased collagen contentment after treatment.

Figure 5

Histopathology of skin and of subcutaneous fat tissue. a) Hematoxylin Eosin stain (HE, nuclei: blue; cytoplasma and connective tissue: red-pink), b) Elastin Van Gieson stain with Resorcin-Fuchsin (EVG, elastic fibers: black, collagen: red, muscle tissue: yellow). One characteristic and representative slide taken from the central (ESW-treated) part of the skin-sample (surface: 75 mm*28 mm, depth: 40 mm, evenly spaced slides) and a corresponding slide (control) of the not treated skin-sample (surface: 70 mm*25 mm, depth 40 mm). Photographs focusing (i) epidermis/dermis/subcutis (4×-objective), (ii) epidermis/dermis (10×-objective), (iii) subcutis (10×-objective). Note: Magnification of each image indicated by bar. No signs of tissue repair are visible – such signs of a response to an injury would be tissue-necrosis, extravasation of erythrocytes, the infiltration of neutrophils lymphocytes and macrophages and the subsequent scar-formation. However an increase of the skin’s connective tissue, the extracellular matrix, particularly collagen and possibly elastin is observed resulting in increased thickness of the dermis and of the scaffolding within the subcutaneous fat tissue.

Figure 5

Histopathology of skin and of subcutaneous fat tissue. a) Hematoxylin Eosin stain (HE, nuclei: blue; cytoplasma and connective tissue: red-pink), b) Elastin Van Gieson stain with Resorcin-Fuchsin (EVG, elastic fibers: black, collagen: red, muscle tissue: yellow). One characteristic and representative slide taken from the central (ESW-treated) part of the skin-sample (surface: 75 mm*28 mm, depth: 40 mm, evenly spaced slides) and a corresponding slide (control) of the not treated skin-sample (surface: 70 mm*25 mm, depth 40 mm). Photographs focusing (i) epidermis/dermis/subcutis (4×-objective), (ii) epidermis/dermis (10×-objective), (iii) subcutis (10×-objective). Note: Magnification of each image indicated by bar. No signs of tissue repair are visible – such signs of a response to an injury would be tissue-necrosis, extravasation of erythrocytes, the infiltration of neutrophils lymphocytes and macrophages and the subsequent scar-formation. However an increase of the skin’s connective tissue, the extracellular matrix, particularly collagen and possibly elastin is observed resulting in increased thickness of the dermis and of the scaffolding within the subcutaneous fat tissue.